Coronary Calcium Scoring Improves Risk Prediction in Patients With Suspected Obstructive Coronary Artery Disease.

Background: In patients with suspected obstructive coronary artery disease (CAD), the risk factor-weighted clinical likelihood (RF-CL) model and the coronary artery calcium score-weighted clinical likelihood (CACS-CL) model improves the identification of obstructive CAD compared with basic pretest probability (PTP) models.
Objectives: The aim of this study was to assess the prognostic value of the new models.
Methods: The incidences of myocardial infarction and death were stratified according to categories by the RF-CL and CACS-CL and compared with categories by the PTP model. We used cohorts from a Danish register (n = 41,177) and a North American randomized study (n = 3,952). All patients were symptomatic and were referred for diagnostic testing because of clinical indications.
Results: Despite substantial down-reclassification of patients to a likelihood ≤5% of CAD with either the RF-CL (45%) or CACS-CL (60%) models compared with the PTP (18%), the annualized event rates of myocardial infarction and death were low using all 3 models; RF-CL 0.51% (95% CI: 0.46-0.56), CACS-CL 0.48% (95% CI: 0.44-0.56), and PTP 0.37% (95% CI: 0.31-0.44), respectively. Overall, comparison of the predictive power of the 3 models using Harrell's C-statistics demonstrated superiority of the RF-CL (0.64 [95% CI: 0.63-0.65]) and CACS-CL (0.69 [95% CI: 0.67-0.70]) compared with the PTP model (0.61 [95% CI: 0.60-0.62]).
Conclusions: The simple clinical likelihood models that include classical risk factors or risk factors combined with CACS provide improved risk stratification for myocardial infarction and death compared with the standard PTP model. Hence, the optimized RF-CL and CACS-CL models identify 2.5 and 3.3 times more patients, respectively, who may not benefit from further diagnostic testing.
Competing Interests: Funding Support and Author Disclosures The PROMISE study was supported by grants from the National Heart, Lung, and Blood Institute (R01HL098237, R01HL098236, R01HL098305, and R01HL098235). Dr Winther has received support from the Novo Nordisk Foundation Clinical Emerging Investigator grant (NNF21OC0066981). Drs Schmidt and Bøttcher have received support from Acarix in the form of an institutional research grant. Dr Schmidt is a part-time consultant for Acarix. Dr Schmidt is a minor shareholder in Acarix. Dr Foldyna has received unrelated research support from National Institutes of Health/National Heart, Lung, and Blood Institute (1R01HL146145-01A1), AstraZeneca, Medtrace Pharma A/C, and Eli Lilly. Dr Hoffmann has received research grants on behalf of Massachusetts General Hospital outside of the submitted work from KOWA Inc, Medimmune LLC, AstraZeneca, and HeartFlow Inc; and has received consultant fees from DCRI and Recor outside of the scope of the submitted work. Dr Knuuti has received speaker fees from GE Healthcare, Merck, Lundbeck, Boehringer Ingelheim, Bayer, and Pfizer; and has received study protocol consultant fees from GE Healthcare and AstraZeneca outside of the submitted work. Dr Bøttcher has participated on Advisory Boards for Novo Nordisk, AstraZeneca, Bayer, Sanofi, and Acarix outside of the submitted work. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
(Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)